Iliofemoral stenting for venous occlusive disease.

BACKGROUND: Venous hypertension is a significant cause of patient morbidity and decreased quality of life. Common etiologies of venous hypertension include deep venous thrombosis (DVT) or congenital abnormalities resulting in chronic outflow obstruction. We have implemented an aggressive endovascular approach for the treatment of iliac venous occlusion with angioplasty and stenting. The purpose of this study was to determine the patency rates with this approach at a large tertiary care center. MATERIALS/METHODS: All patients undergoing iliofemoral venous angioplasty and stenting over a 4-year period were identified from a vascular surgical registry. Charts were reviewed retrospectively for patient demographics, the extent of venous system involvement, the time course of the venous pathology, and any underlying cause. Technical aspects of the procedure including previous angioplasty or stenting attempts and presence of collaterals on completion venogram were then recorded. Patency upon follow-up was determined using primarily ultrasound scans; other imaging methods were used if patency was not clear using an ultrasound scan. RESULTS: A total of 36 patients (40 limbs) were stented from January 2005 through December 2008. Of these patients, 27 were women (75%). Both lower extremities were involved in 4 patients. Thrombolysis was performed in 19 patients (52.8%). Thrombosis was considered acute (<30 days) in 13 patients (38%). The majority of patients who had a recognized underlying etiology were diagnosed with May-Thurner syndrome (15 patients; 42%). In 9 patients, an etiology was not determined (25%). The mean follow-up time period in the study population was 10.5 months. One stent in the study occluded acutely and required restenting. Primary patency rates at 6, 12, and 24 months were 88% (75.2-100), 78.3% (61.1-95.4), and 78.3% (61.1-95.4), respectively. Secondary patency rates for the same time frames were 100% (100.0, 100.0), 95% (85.4, 100.0), and 95% (85.4, 100.0). Better outcomes were seen in stenting for May-Thurner syndrome and idiopathic causes, whereas external compression and thrombophilia seemed to portend less favorable outcomes (P < .001). Symptomatic improvement was reported in 24 of 29 patients (83%) contacted by telephone follow-up. CONCLUSION: Iliofemoral venous stenting provides a safe and effective option for the treatment of iliac venous occlusive disease. Acceptable patency rates can be expected through short-term follow-up, especially in the case of May-Thurner syndrome. Further experience with this approach and longer-term follow-up is necessary. Thrombophilia workup should be pursued aggressively in this population, and further studies should be undertaken to determine the optimal length of anticoagulation therapy after stent placement.

The azygos system as a rare alternative for chronic indwelling catheters placement.

Chronic indwelling catheters are plagued with a high rate of complications, including infection, central venous occlusion, or thrombosis. When direct access to the superior or inferior vena cava is not possible, venography may identify alternatives that might be viable with current endovascular techniques. This case report describes the successful placement of a tunneled catheter for total parenteral nutrition in the azygos arch through a small collateral vein from the left jugular vein in a patient with no other alternatives because of superior vena cava occlusion and inferior vena cava thrombophlebitis.

Endovascular management of chronic infrarenal aortic occlusion.

PURPOSE: To review our experience with the endovascular treatment of chronic infrarenal aortic occlusion with regard to technical success and midterm patency, as well as perioperative mortality and morbidity. METHODS: A retrospective review was performed of patients who presented from January 1, 2000, to December 31, 2005, with a diagnosis of chronic infrarenal aortic occlusion (TASC D) treated with endovascular techniques. In this time period, 31 patients (22 women; mean age 63 years) underwent attempted recanalization of the occluded aorta and iliac arteries. Claudication was the most common presenting symptom (14, 45%). Patients were treated solely with angioplasty and stenting or thrombolysis followed by angioplasty/stenting based on surgeon preference. RESULTS: Technical success was 93%. The 2 failures were individual cases of wire-induced iliac artery perforation and failed access; both patients were treated with bypass grafting. Nine (29%) patients had thrombolysis prior to angioplasty. There were no perioperative deaths. Postoperative ankle-brachial indexes increased significantly from preoperative values (p<0.0001). There were 3 technical complications: 1 (3%) iatrogenic iliac artery injury and 2 (6%) perioperative limb thromboses requiring intervention. Other complications included 6 (19%) access site events and 5 (16%) episodes of acute renal dysfunction, 2 requiring permanent dialysis. Over a mean follow-up of 12 months, there was no limb loss. At 1 and 3 years, the primary/secondary patency rates were 85%/100% and 66%/90%, respectively. CONCLUSION: Endovascular therapy for chronic infrarenal aortic occlusion has a high technical success rate, with good midterm primary and secondary patency rates. However, renal dysfunction can occur; the etiology is likely multifactorial from contrast volumes, embolization, and/or renal arterial disease.

The brachial artery: a critical access for endovascular procedures.

OBJECTIVE: The brachial artery is often used for coronary angiography. However, data on brachial access for aortic and peripheral interventions are limited. This study evaluated our experience with brachial artery catheterization for diagnostic arteriography and endovascular interventions. METHODS: Between August 2004 and August 2005, 2026 endovascular procedures were performed. Of these, 323 cases (16%) in 289 patients required brachial artery access, forming the basis for this study. Patients who underwent multiple interventions, but with a single access (ie, thrombolysis), were considered a single case. Demographic and clinical data were recorded in a database and analyzed using logistic regression analyses with generalized estimating equations and the Fisher exact test for nominal variables. RESULTS: The mean age of all patients was 66.4 years, with 57% men. Brachial access was used for diagnostic purposes in 27% and for interventions including angioplasty, stenting, and thrombolysis in 73%. The use of brachial access was considered obligatory in 40%, adjunctive in 19% (ie, endovascular repair of abdominal aortic and thoracic aortic aneurysms) and preferential to femoral access in 41%. In 91% of patients, the brachial arteries were accessed percutaneously, and 9% underwent surgical cutdown for access. In patients whose brachial artery was approached percutaneously, access was achieved in all but one (99.6% technical success rate). Hemostasis after catheterization was achieved by manual compression in 89%. Operative mortality rate was 6.2% and not related to brachial artery access. Brachial access site-related complications occurred in 21 patients (6.5%). Thirteen of these 21 patients (62%) required a surgical correction, mostly for brachial artery thrombosis or pseudoaneurysm. Patients with complications were more commonly women (odds ratio [OR], 4.7; 95% confidence interval [CI], 1.68-13.26; P = .003) and had a long interventional sheath (OR, 6.7; 95% CI, 1.53-29.07; P = .012). The risk of a brachial artery complication was not associated with thrombolysis, procedure type, vascular territory treated, or the use of heparin. No upper extremity limb or finger loss occurred. CONCLUSIONS: Brachial artery access is necessary for complex endovascular procedures and can be achieved in most patients safely. Postprocedural vigilance is warranted because most patients with complications will require operative correction.

Alfimeprase for the treatment of acute peripheral arterial occlusion.

BACKGROUND: Catheter-directed thrombolysis for the management of acute peripheral arterial occlusion emerged as a viable treatment option in the 1990s. It offers a less invasive approach than traditional open surgery for correcting acute limb ischemia. Nonetheless, thrombolysis is plagued by a relatively high rate of bleeding complications as well as long infusion times. OBJECTIVE: To review the clinical experience with alfimeprase, a new thrombolytic agent. METHODS: All published data on alfimeprase were reviewed. Review articles, press releases and web-based data were also included. RESULTS/CONCLUSIONS: Alfimeprase is a novel agent with a unique mechanism of action compared with currently available thrombolytic agents. It is a direct-acting fibrinolytic agent that does not require activation of plasminogen. This mechanism may potentially reduce the number of bleeding complications. Current clinical data are limited, but ongoing clinical trials may demonstrate that this compelling agent represents a clinical advance.

Barriers to endovascular aortic aneurysm repair: past experience and implications for future device development.

Despite improvements in endovascular aortic aneurysm repair (EVAR) devices and techniques, significant anatomic constraints still preclude successful EVAR in a large number of patients. The authors sought to identify the current barriers to EVAR and examine their evolution over time. Patients were evaluated for potential endovascular repair by computed tomography angiography (CTA) with or without supplemental conventional arteriograms. The patient population was separated into 2 groups (A and B) based on early and late time periods in the experience with EVAR, corresponding to the availability of various devices. Group A (early) consisted of the Guidant Ancure, Medtronic Talent, and AneuRx devices and comprised patients presenting between April 1997 through June 2000. Group B (late) consisted of the Medtronic AneuRx, Cook Zenith, Edwards Lifepath, Gore Excluder, and Endologix PowerLink devices and comprised patients presenting between July 2000 and December 2003. Patient demographics and anatomic reasons for rejection were recorded in a database for statistical analysis. In total, 547 patients were evaluated (463 men, 84 women). Of these, 346 patients (63%; 312 men, 34 women) were deemed suitable candidates for EVAR and 201 (37%; 151 men, 50 women) were rejected. There was no significant difference in the overall rate of rejection in the early vs the late time period (34% A, 41% B, p = 0.08), but the number of exclusion criteria per patient decreased over time; patients rejected for EVAR had an overall average of 1.6 exclusion criteria (Group A, 1.9; Group B, 1.2). The reasons for rejection did significantly change over time. Specifically, rejection on the basis of inadequate arterial access, presence of extensive iliac artery aneurysms, or an inadequate proximal neck decreased. A disproportionate number of women were excluded throughout the study: Group A, 56% of women compared to 30% of men (p = 0.0003); Group B, 63% of women compared to 36% of men (p = 0.0022). Women were more likely than men to have inadequate arterial access routes. In addition, patients with high operative risk were also more likely to be excluded from EVAR, a finding that persisted over time. Anatomic constraints continue to pose significant challenges to aortic endografting. Progress has been made in that technological advances have conquered some of the previous anatomic challenges, chiefly those of arterial access and treatment of concomitant iliac aneurysm disease. However, the overall rate of rejection for EVAR remains the same. The chief anatomic barriers continue to be the difficult aortic neck and management of branched vascular segments.

Stromal cell-derived factor and granulocyte-monocyte colony-stimulating factor form a combined neovasculogenic therapy for ischemic cardiomyopathy.

OBJECTIVE: Ischemic heart failure is an increasingly prevalent global health concern with major morbidity and mortality. Currently, therapies are limited, and novel revascularization methods might have a role. This study examined enhancing endogenous myocardial revascularization by expanding bone marrow-derived endothelial progenitor cells with the marrow stimulant granulocyte-monocyte colony-stimulating factor and recruiting the endothelial progenitor cells with intramyocardial administration of the potent endothelial progenitor cell chemokine stromal cell-derived factor. METHODS: Ischemic cardiomyopathy was induced in Lewis rats (n = 40) through left anterior descending coronary artery ligation. After 3 weeks, animals were randomized into 4 groups: saline control, granulocyte-monocyte colony-stimulating factor only (GM-CSF only), stromal cell-derived factor only (SDF only), and combined stromal cell-derived factor/granulocyte-monocyte colony-stimulating factor (SDF/GM-CSF) (n = 10 each). After another 3 weeks, hearts were analyzed for endothelial progenitor cell density by endothelial progenitor cell marker colocalization immunohistochemistry, vasculogenesis by von Willebrand immunohistochemistry, ventricular geometry by hematoxylin-and-eosin microscopy, and in vivo myocardial function with an intracavitary pressure-volume conductance microcatheter. RESULTS: The saline control, GM-CSF only, and SDF only groups were equivalent. Compared with the saline control group, animals in the SDF/GM-CSF group exhibited increased endothelial progenitor cell density (21.7 +/- 3.2 vs 9.6 +/- 3.1 CD34 + /vascular endothelial growth factor receptor 2-positive cells per high-power field, P = .01). There was enhanced vascularity (44.1 +/- 5.5 versus 23.8 +/- 2.2 von Willebrand factor-positive vessels per high-power field, P = .007). SDF/GM-CSF group animals experienced less adverse ventricular remodeling, as manifested by less cavitary dilatation (9.8 +/- 0.1 mm vs 10.1 +/- 0.1 mm [control], P = .04) and increased border-zone wall thickness (1.78 +/- 0.19 vs 1.41 +/- 0.16 mm [control], P = .03). (SDF/GM-CSF group animals had improved cardiac function compared with animals in the saline control group (maximum pressure: 93.9 +/- 3.2 vs 71.7 +/- 3.1 mm Hg, P < .001; maximum dP/dt: 3513 +/- 303 vs 2602 +/- 201 mm Hg/s, P < .05; cardiac output: 21.3 +/- 2.7 vs 13.3 +/- 1.3 mL/min, P < .01; end-systolic pressure-volume relationship slope: 1.7 +/- 0.4 vs 0.5 +/- 0.2 mm Hg/microL, P < .01.) CONCLUSION: This novel revascularization strategy of bone marrow stimulation and intramyocardial delivery of the endothelial progenitor cell chemokine stromal cell-derived factor yielded significantly enhanced myocardial endothelial progenitor cell density, vasculogenesis, geometric preservation, and contractility in a model of ischemic cardiomyopathy.

Targeted overexpression of leukemia inhibitory factor to preserve myocardium in a rat model of postinfarction heart failure.

OBJECTIVE: Myocardial infarction leads to cardiomyocyte loss. The cytokine leukemia inhibitory factor regulates the differentiation and growth of embryonic and adult heart tissue. This study examined the effects of gene transfer of leukemia inhibitory factor in infarcted rat hearts. METHODS: Lewis rats underwent ligation of the left anterior descending coronary artery and direct injection of adenovirus encoding leukemia inhibitory factor (n = 10) or null transgene as control (n = 10) into the myocardium bordering the ischemic area. A sham operation group (n = 10) underwent thoracotomy without ligation. After 6 weeks, the following parameters were evaluated: cardiac function with a pressure-volume conductance catheter, left ventricular geometry and architecture by histologic methods; myocardial fibrosis by Masson trichrome staining, apoptosis by terminal deoxynucleotidal transferase-mediated deoxyuridine triphosphate nick-end labeling assay, and cardiomyocyte size by immunofluorescence. RESULTS: Rats with overexpression of leukemia inhibitory factor had more preserved myocardium and less fibrosis in both the infarct and its border zone. The border zone in leukemia inhibitory factor-treated animals contained fewer apoptotic nuclei (1.6% +/- 0.1% vs 3.3% +/- 0.2%, P < .05) than that in control animals and demonstrated cardiomyocytes with larger cross-sectional areas (910 +/- 60 microm 2 vs 480 +/- 30 microm 2 , P < .05). Leukemia inhibitory factor-treated animals had increased left ventricular wall thickness (2.1 +/- 0.1 mm vs 1.8 +/- 0.1 mm, P < .05) and less dilation of the left ventricular cavity (237 +/- 22 microL vs 301 +/- 16 microL, P < .05). They also had improved cardiac function, as measured by maximum change in pressure over time (3950 +/- 360 mm Hg/s vs 2750 +/- 230 mm Hg/s, P < .05) and the slopes of the maximum change in pressure over time-end-diastolic volume relationship (68 +/- 5 mm Hg/[s . microL] vs 46 +/- 6 mm Hg/[s . microL], P < .05) and the preload recruitable stroke work relationship (89 +/- 10 mm Hg vs 44 +/- 4 mm Hg, P < .05). CONCLUSIONS: Myocardial gene transfer of leukemia inhibitory factor preserved cardiac tissue, geometry, and function after myocardial infarction in rats.

Administration of a tumor necrosis factor inhibitor at the time of myocardial infarction attenuates subsequent ventricular remodeling.

BACKGROUND: Tumor necrosis factor (TNF) causes myocardial extracellular matrix remodeling and fibrosis in myocardial infarction and chronic heart failure models. Pre-clinical and clinical trials of TNF inhibition in chronic heart failure have shown conflicting results. This study examined the effects of the administration of a TNF inhibitor immediately after myocardial infarction on the development of heart failure. METHODS: Lewis rats underwent coronary artery ligation and then received either intravenous etanercept (n = 14), a soluble dimerized TNF receptor that inhibits TNF, or saline as control (n = 13). Leukocyte infiltration into the infarct borderzone was evaluated 4 days post-ligation in 7 animals (etanercept = 4, control = 3). After 6 weeks, the following parameters were evaluated in the remaining animals: cardiac function with a pressure-volume conductance catheter, left ventricular (LV) geometry, and borderzone collagenase activity. RESULTS: Etanercept rats had significantly less borderzone leukocyte infiltration 4 days post-infarction than controls (10.7 +/- 0.5 vs 18.0, +/-2.0 cells/high power field; p < 0.05). At 6 weeks, TNF inhibition resulted in significantly reduced borderzone collagenase activity (110 +/- 30 vs 470 +/- 140 activity units; p < 0.05) and increased LV wall thickness (2.1 +/- 0.1 vs 1.8 +/- 0.1 mm, p < 0.05). Etanercept rats had better systolic function as measured by maximum LV pressure (84 +/- 3 mm Hg vs 68 +/- 5 mm Hg, p < 0.05) and the maximum change in left ventricular pressure over time (maximum dP/dt) (3,110 +/- 230 vs 2,260 +/- 190 mm Hg/sec, p < 0.05), and better diastolic function as measured by minimum dP/dt (-3,060 +/- 240 vs -1,860 +/- 230 mm Hg/sec; p < 0.05) and the relaxation time constant (14.6 +/- 0.6 vs 17.9 +/- 1.2 msec; p < 0.05). CONCLUSIONS: TNF inhibition after infarction reduced leukocyte infiltration and extracellular matrix turnover and preserved cardiac function.